In silico interactions of statins with cell death-inducing DNA fragmentation factor-like effector A (CIDEA)

Statins are the low-density lipoproteins (LDL)-cholesterol-lowering drugs of first choice and used to prevent increased risk cardiovascular cerebrovascular diseases. Although some their effects well known, little is known about ability regulate other lipid-related proteins which control apoptotic mechanisms. The aim this study was explore whether statins can bind cell death-inducing DNA fragmentation factor-like effector A (CIDEA), might be a possible pleiotropic mechanism action these on modulation apoptosis lipid metabolism. structures were subjected molecular docking dynamics with human CIDEA protein investigate interaction pattern identify residues important. results indicated that atorvastatin rosuvastatin showed best energy (?8.51 ?8.04 kcal/mol, respectively) followed by fluvastatin (?7.39), pitavastatin (?6.5), lovastatin (?6.23), pravastatin (?6.04) simvastatin (?5.29). Atorvastatin further at 50 ns suggested rosuvastatin-CIDEA complex had lower root-mean square deviation fluctuation when compared atorvastatin-CIDEA. Since two arginine -ARG19 ARG22-were identified common for CIDEA, single-point mutation induced in determine they important binding interaction. Mutation seemed affect mostly suggesting therefore indicate another metabolic statin. • promotes homeostasis cross talking endoplasmic reticulum droplets. FDA-approved cholesterol levels, but much role still unknown. In silico interacted through ARG19 ARG22. ARG22 affected most CIDEA-atorvastatin complex. CIDEA-rosuvastatin RMSD RMSF, better stability compactness.